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Phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

What condition is giant cell arteritis associated with?

A

Polymyalgia rheumatica

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2
Q

Causes of cauda equina syndrome?

A
  • herniated disc
  • tumours (metastasis)
  • spondylolisthesis (anterior displacement of a vertebra)
  • abscess
  • trauma
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3
Q

What do the nerves of the cauda equina supply?

A
  • sensation to the perineum, bladder and rectum
  • motor innervation to lower limbs and anal & urethral sphincters
  • parasympathetic innervation of the bladder and rectum
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4
Q

Nerve roots of the cauda equina?

A
  • L3-5
  • S1-5
  • coccygeal nerves
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5
Q

Red flags for cauda equina syndrome?

A
  • saddle anaesthesia (perineum)
  • loss of sensation in bladder / rectum
  • urinary retention / incontinence
  • faecal incontinence
  • bilateral sciatica
  • bilateral / severe motor weakness in legs
  • reduced anal tone
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6
Q

Mechanism of action of neostigmine / pyridostigmine?

A

Blocks active site of acetylcholinesterase, increasing the amount of acetylcholine available to the post-synaptic membrane.

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7
Q

What is alteplase?

A

Thrombolytic drug used to treat acute ischaemic stroke (also STEMI and PE).

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8
Q

Mechanism of action of alteplase?

A

Converts plasminogen to plasmin, resulting in the lysis of fibrin.

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9
Q

Recommended time window for alteplase after acute ischaemic stroke?

A

< 4.5 after symptom onset.

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10
Q

What type of haemorrhage has a lucid interval?

A

Extradural haemorrhage

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11
Q

Triggering factors for migraine?

A
  • CHeese
  • Oral contraceptive pill
  • Caffeine
  • alcohOL
  • Anxiety
  • Travel
  • Exercise
  • (chocolate)
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12
Q

First line investigation for ischaemic stroke?

A

CT head

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13
Q

Definition of ischaemic stroke?

A

Rapid onset of neurological impairment, lasting greater than 24 hours (or leading to death). Due to reduced / absent blood supply to an area of the brain leading to death of tissues.

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14
Q

Initial treatment for ischaemic stroke?

A

300mg aspirin

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15
Q

What is the pathophysiology of Parkinson’s disease?

A
  • progressive neurodegeneration of dopaminergic neurones in the substantia nigra
  • this leads to dopamine deficiency, resulting in impaired initiation of movements
  • aggregation of alpha-synuclein forms Lewy bodies
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16
Q

Signs of Parkinson’s?

A
  • bradykinesia
  • rigidity
  • resting tremor
  • postural instability
  • shuffling gait
  • expressionless face
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17
Q

Eye movement disorder in Parkinson’s

A

Conjugate gaze disorder

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18
Q

How is Parkinson’s investigated?

A
  • PET scan with fluorodopa (shows decreased dopamine uptake in the substantia nigra)
  • MRI brain
  • DaTscan (type of SPECT to distinguish between Parkinson’s and essential tremor)
  • serum ceruloplasmin / 24 hr urinary copper (exclude Wilson’s disease)
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19
Q

What is SPECT?

A

single-photon emission computed tomography

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20
Q

What is PET?

A

positron emission tomography

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21
Q

Differentials for Parkinson’s?

A
  • Wilson’s disease
  • essential tremor
  • drug-induced parkinsonism
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22
Q

Pharmacological management of Parkinson’s?

A
  • Levodopa (converted to dopamine)
  • dopamine agonists
  • MAO-B (monoamine oxidase) inhibitors
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23
Q

Non-pharmacological management of Parkinson’s?

A
  • deep brain stimulation
  • physiotherapy
  • speech and language therapy
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24
Q

Complications of Parkinson’s?

A
  • dementia
  • depression
  • sleep disorders
  • falls
  • dyskinesia due to medications
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25
Q

In what population of patients should sodium valproate not be used for seizures?

A

Females of child-bearing age, due to teratogenic effects.

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26
Q

First line treatment for new onset GTCS?

A
  • lamotrigine
  • topiramate
  • oxcarbazepine
  • levetiracetam
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27
Q

Side effects of long term levodopa use?

A

dyskinesia

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28
Q

Initial investigation for subarachnoid haemorrhage?

A

CT head

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29
Q

Investigation for SA haemorrhage if CT head is negative?

A

lumbar puncture

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30
Q

How is Guillain-Barre syndrome treated?

A
  • IV immunoglobulin

- plasmapheresis (plasma exchange)

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31
Q

What is the only disease-modifying drug for MND?

A

Riluzole (anti-glutamate medication).

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32
Q

Investigations for myasthenia gravis?

A
  • serum anti-AChR antibodies / anti-MuSK antibodies
  • repetitive nerve stimulation
  • ice pack test (improves ptosis)
  • CT / MRI chest - thymus gland assessment
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33
Q

How is the thymus involved in myasthenia gravis?

A
  • 70% of patients have thymic follicular hyperplasia

- 10% have thymoma

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34
Q

Initial presentation of myasthenia gravis vs LEMS?

A
  • in myasthenia gravis, extra-ocular involvement is the most common initial presentation
  • in LEMS, weakness of limbs is the most common initial presentation
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35
Q

Definition of transient ischaemic attack?

A

A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia without acute infarction.
Sudden onset, lasts from a few minutes to 24 hours.

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36
Q

What is meant by crescendo TIA?

A

2 or more TIAs in a week - has a high risk of developing into stroke.

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37
Q

What causes TIA?

A
  • thrombosis - due to atherosclerosis or small vessel disease (sickle cell anaemia, vasculitis)
  • emboli - due to AF or carotid artery disease
  • dissection (usually carotid) - may be spontaneous or secondary to trauma
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38
Q

Risk factors for TIA?

A
  • smoking
  • diabetes
  • hypertension
  • hypercholesterolaemia
  • obesity
  • AF
  • carotid artery disease
  • advancing age
  • thrombophilic disorders (anti-phospholipid syndrome)
  • sickle cell anaemia
  • vasculitis
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39
Q

Pathophysiology of TIA?

A

Transient reduction in blood flow to an area of cerebral tissue, resulting in ischaemia causing focal neurological symptoms.

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40
Q

Clinical manifestations of TIA?

A
  • unilateral muscle weakness
  • unilateral sensory loss
  • dysphasia
  • ataxia / incoordination / vertigo
  • amaurosis fugax
  • homonymous hemianopia
  • cranial nerve palsies
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41
Q

Investigations for TIA?

A
  • clinical diagnosis
  • head CT / MRI to rule out haemorrhage or infarction
  • ABCD2 score to calculate stroke risk
  • carotid dopplers (if patient is a candidate for carotid endarterectomy)
  • lipid profile
  • clotting profile (prothrombin time)
  • ECG
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42
Q

What is the ABCD2 score?

A

Estimates risk of stroke following TIA.

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43
Q

Differentials for TIA?

A
  • stroke
  • hypoglycaemia
  • seizure with Todd’s paralysis
  • complex migraine
  • space-occupying lesion
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44
Q

Acute TIA management?

A
  • assessment in specialist clinic on the day / next day
  • calculate stroke risk (ABCD2 score)
  • 300mg aspirin for 2 weeks
  • DOAC for AF (instead of aspirin)
  • consider carotid stenting / endarterectomy
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45
Q

What is carotid endarterectomy?

A

Surgery to remove plaque within carotid arteries?

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46
Q

When is carotid endarterectomy indicated?

A

If carotid artery is over 70% stenosed.

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47
Q

Long term prevention after TIA?

A
  • 75mg clopidogrel (after two weeks of aspirin)
  • anti-hypertensives
  • statin therapy
  • diabetic control
  • lifestyle measures (physical activity, smoking cessation, diet optimisation, reduce alcohol)
  • stop driving
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48
Q

Complications of TIA?

A
  • stroke

- MI

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49
Q

How many TIA patients go on to have a stroke?

A

Over 10% within 3 months.

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50
Q

What is amaurosis fugax?

A

Temporary painless blindness affecting one eye, as a result of ischaemia.

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51
Q

Aetiology of amaurosis fugax?

A
  • obstruction of the ophthalmic artery / central retinal artery (branch of the ICA) due to atherosclerotic emboli
  • optic neuritis
  • giant cell arteritis
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52
Q

Risk factors for amaurosis fugax?

A
  • TIA risk factors (smoking, hypertension, etc)

- giant cell arteritis

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53
Q

Clinical manifestations of amaurosis fugax?

A

‘Black curtain’ comes across the vision.

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54
Q

Investigations for amaurosis fugax?

A
  • eye examination
  • carotid doppler ultrasound
  • MR / CT angiography
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55
Q

Management of amaurosis fugax?

A
  • control risk factors (statin therapy, anti-hypertensives. diabetes control)
  • anticoagulation therapy (aspirin / clopidogrel)
  • carotid stenting / endarterectomy
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56
Q

What is meant by stroke?

A

Cerebrovascular event caused by reduced / absent blood flow to cerebral tissue, resulting in tissue death. Characterised by sudden onset of focal neurological signs lasting longer than 24 hours.

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57
Q

What is the split between ischaemic and haemorrhagic stroke?

A
  • ischaemic 85%

- haemorrhagic 15%

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58
Q

Causes of haemorrhagic stroke?

A
  • hypertension
  • trauma
  • anticoagulation
  • tumour
  • AV malformation
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59
Q

Most common cause of haemorrhagic stroke?

A

hypertension

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60
Q

Causes of ischaemic stroke?

A
  • thrombosis (atherosclerosis or small vessel disease - vasculitis / sickle cell disease)
  • emboli (AF or carotid artery disease)
  • dissection (carotid), either spontaneous or secondary to trauma
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61
Q

How does carotid dissection result in ischaemic stroke?

A

Forms an intramural haematoma that compromises blood flow.

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62
Q

Risk factors for stroke?

A
  • older age
  • hypertension
  • smoking
  • diabetes
  • hypercholesterolaemia
  • obesity
  • AF
  • carotid artery disease
  • thrombophilic disorders
  • sickle cell disease
  • vasculitis
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63
Q

Clinical manifestations of a stroke affecting the carotid territory?

A
  • contralateral face / arm / leg weakness
  • contralateral sensory loss
  • dysphasia
  • dysarthria
  • homonymous hemianopia
  • higher cortical dysfunction
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64
Q

Clinical manifestations of a stroke affecting the posterior circulation territory?

A
  • ataxia
  • dizziness
  • dysarthria
  • diplopia
  • diplegia - paralysis affecting symmetrical parts of the body
  • cranial nerve palsies
  • visual field defects
  • isolated homonymous hemianopia
  • reduced GCS
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65
Q

Clinical manifestations of a lacunar stroke?

A
  • motor hemiparesis
  • ataxic hemiparesis
  • ‘clumsy hand’
  • dysarthria
    May be pure hemisensory, pure motor hemiparesis or mixed sensorimotor.
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66
Q

Clinical manifestations of a haemorrhagic stroke?

A

More likely to present with global features:

  • focal neurological deficitis
  • headache
  • altered mental status
  • nausea and vomiting
  • seizures
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67
Q

Investigations for stroke?

A
  • CT head (sensitive for haemorrhage, usually cannot diagnose acute phase infarct)
  • MRI brain
  • perfusion imaging (CT angiography) to check viable tissue and avoid reperfusion injury
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68
Q

Differentials for stroke?

A
  • TIA
  • seizure with Todd’s paresis
  • tumour / abscess
  • migraine
  • hypoglycaemia
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69
Q

Acute management of ischaemic stroke?

A
  • aspirin 300mg (for 2 weeks)
  • admit to specialist stroke unit
  • IV alteplase for thrombolysis (within 4.5 hours)
  • thrombectomy (within 6 hours)
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70
Q

What is the mechanism of action of alteplase?

A

Tissue plasminogen activator - produces plasmin that lyses fibrin.

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71
Q

Contraindications to alteplase?

A
  • major recent surgery
  • bleeding
  • severe hypertension
  • brain malignancies
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72
Q

Long term management of ischaemic stroke?

A
  • lifestyle changes & stop driving
  • occupational therapy & rehabilitation
  • clopidogrel 75mg lifelong (after 2 weeks aspirin)
  • DOAC for AF
  • antihypertensives & statin therapy
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73
Q

Management of haemorrhagic stroke?

A
  • ABCDE, monitor pupil responses and GCS
  • correct coagulopathy / reverse anticoagulation
  • BP control (acutely aim for < 140-160 systolic)
  • neurosurgery
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74
Q

Early complications of stroke?

A
  • seizures
  • cerebral oedema
  • death
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75
Q

Late complications of stroke?

A
  • motor and sensory deficits
  • bladder and bowel dysfunction
  • cognitive problems
  • visual problems
  • psychological problems
  • swallowing difficulties
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76
Q

What is a subarachnoid haemorrhage?

A

Sudden severe headache (‘thunderclap headache’) due to bleeding into the subarachnoid space.

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77
Q

Causes of SA haemorrhage?

A
  • trauma
  • aneurysm rupture
  • AV malformation
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78
Q

Risk factors for SA haemorrhage?

A
  • age > 50
  • female
  • smoking
  • hypertension
  • connective tissue disorders (Marfan’s / EDS)
  • family history
  • polycystic kidney disease
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79
Q

Clinical manifestations of SA haemorrhage?

A
  • severe sudden onset ‘thunderclap’ headache
  • impaired / loss of consciousness
  • meningismus (neck stiffness, muscle aches)
  • photophobia
  • nausea and vomiting
  • Kernig’s and Brudzinski’s signs
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80
Q

Investigations for SA haemorrhage?

A
  • CT head shows hyperdense areas in SA space

- lumbar puncture if CT is negative, shows bloody CSF (performed at least 12 hrs after symptom onset)

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81
Q

Management of SA haemorrhage?

A
  • supportive care: intubation and sedation may be required, O2, analgesia
  • nimodipine (CCB to prevent delayed cerebral ischaemia)
  • neurosurgery (endovascular coiling, surgical clipping)
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82
Q

Complications of SA haemorrhage?

A
  • obstructive hydrocephalus
  • arterial vasospasm
  • re-bleeding of aneurysm
  • long-term neurological deficits
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83
Q

What causes delayed cerebral ischaemia in SA haemorrhage?

A

Arterial vasospam

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84
Q

Mortality from SA haemorrhage?

A

50%

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85
Q

What is a subdural haemorrhage?

A

Collection of blood between the dura mater and arachnoid mater.

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86
Q

Over what time frame may a subdural haemorrhage occur?

A
  • acute (< 3 days)
  • subacute (3-21 days)
  • chronic (21 days)
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87
Q

Causes of subdural haemorrhage?

A
  • trauma (temporal side of head, causes rupture of bridging veins)
  • cerebral aneurysm rupture
  • AV malformation rupture
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88
Q

Risk factors for subdural haemorrhage?

A
  • history of trauma / loss of consciousness
  • vulnerability to falls (dementia)
  • age > 65
  • anticoagulation / coagulopathy
  • alcohol misuse
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89
Q

Pathophysiology of subdural haemorrhage?

A
  • haematoma volume increases, causing compression and displacement of the brain parenchyma
  • ICP rises, which may lead to brain herniation
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90
Q

Clinical manifestations of subdural haemorrhage?

A

Gradual deterioration:

  • headache
  • nausea and vomiting
  • impaired consciousness / confusion
  • ataxia / poor balance
  • cranial nerve palsies
  • seizures
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91
Q

Investigations for subdural haemorrhage?

A
  • non-contrast CT head (shows crescent shaped collection of blood)
  • MRI brain to identify an underlying cause
  • coagulation screen
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92
Q

Acute vs chronic subdural haemorrhage appearance on CT?

A

Acute - hyperdense (white).

Chronic - hypodense.

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93
Q

Management of subdural haemorrhage?

A
  • correct coagulopathy / anticoagulation reversal
  • anticonvulsants
  • conservative management for small bleeds
  • decompressive craniectomy
  • burr hole craniotomy for chronic subdural haemorrhage
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94
Q

Complications of subdural haemorrhage?

A
  • permanent neurological deficits
  • coma
  • seizures
  • intracranial infection
  • recurrent subdural haematoma
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95
Q

What is an extradural haemorrhage?

A

Acute haemorrhage between the dura mater and the inner surface of the skull.

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96
Q

Causes of extradural haemorrhage?

A

Skull trauma in the temporoparietal region (often involves middle meningeal artery) - falls, assault, sporting injuries.
Other causes such as AV malformations and bleeding disorders.

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97
Q

Pathophysiology of extradural haemorrhage?

A
  • as the haematoma grows in volume, it strips the dura mater away from the skull
  • ICP increases, leading to midline shift and tentorial herniation, and eventually brainstem death
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98
Q

Clinical manifestations of extradural haemorrhage?

A

Immediate loss of consciousness, lucid period, then progressive decrease in consciousness.

  • headache
  • nausea and vomiting
  • confusion
  • motor / sensory limb defects
  • cushing’s triad
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99
Q

Investigations for extradural haemorrhage?

A
  • CT head shows lemon shaped haemorrhage with midline shift

- blood glucose (exclude hypoglycaemia)

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100
Q

Management of extradural haemorrhage?

A
  • correct coagulopathy / anticoagulation reversal
  • prophylactic antibiotics
  • anticonvulsants
  • mannitol / barbiturates to reduce ICP
  • burr hole craniotomy
  • decompressive hemicraniectomy for large bleeds
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101
Q

Complications of extradural haemorrhage?

A
  • infection
  • cerebral ischaemia
  • seizures
  • hydrocephalus
  • brainstem injury
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102
Q

What is the definition of epilepsy?

A

Condition characterised by recurrent seizures unprovoked by any immediate identified cause.
2 or more unprovoked seizures separated by at least 24 hours.

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103
Q

What is the definition of an epileptic seizure?

A

Paroxysmal event in which changes of behaviour, sensation, or cognitive processes are caused by excessive, hyper-synchronous neuronal excitation in the brain.

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104
Q

Pathophysiology of epileptic seizures?

A

Abnormal properties of neurons lead to inappropriate hyperexcitability and hypersynchrony.

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105
Q

Initiation of generalised-onset seizures?

A

Bihemispheric electrical discharges.

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106
Q

Initiation of focal-onset generalised seizures?

A

Initially a focal seizure occurs, then the electrical discharges evolve through the ipsilateral hemisphere and cross the corpus callosum to continue in the contralateral hemisphere.

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107
Q

Clinical manifestations of GTCS?

A
  • loss of consciousness
  • tonic phase (muscle tensing) followed by clonic phase (muscle jerking)
  • tongue biting
  • incontinence
  • irregular breathing
  • post-ictal period where patient is confused, drowsy and irritable / depressed
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108
Q

Investigations for GTCS?

A
  • video EEG (shows generalised epileptiform activity)
  • head CT / MRI may show a structural lesion
  • lumbar puncture (elevated WCC in CNS infection)
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109
Q

Differentials for GTCS?

A
  • syncope
  • cardiac arrhythmia
  • transient ischaemic attack
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110
Q

Pharmacological management of GTCS?

A

Monotherapy with an anticonvulsant - try two different drugs before initiating dual therapy.

  • carbamazepine
  • lamotrigine
  • topiramate
  • sodium valproate
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111
Q

Summary of management of GTCS?

A
  • anti-convulsant medication
  • surgical resection (in patients with drug-resistant focal onset epilepsy)
  • deep brain / vagus nerve stimulation
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112
Q

What are focal seizures?

A

Seizures arise in one portion of the brain, commonly the temporal lobe. They may affect hearing, speech, memory and emotions.

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113
Q

Pathophysiology of focal seizures?

A

Hyperexcitability and hypersynchronicity of a group of neurons in one area of the brain.

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114
Q

Clinical manifestations of focal seizures?

A
  • movement of a specific body part
  • sense of premonition (fear, deja vu)
  • automatisms (lip smacking, clothes picking)
  • staring and being unaware of surroundings
  • visual, olfactory or gustatory hallucinations
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115
Q

Investigations for focal seizures?

A
  • video EEG
  • head CT / MRI for structural abnormalities
  • lumbar puncture and CSF fluid analysis for signs of infection
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116
Q

Differentials for focal seizures?

A
  • syncope
  • TIA
  • tic disorders
  • tremor
  • dissociative disorders
  • migraine
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117
Q

Management of acute focal seizures?

A

Benzodiazepines (rectal diazepam, intranasal midazolam, oral lorazepam, IV benzodiazepines in hospital).

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118
Q

Long-term anticonvulsant therapy for focal seizures?

A

Monotherapy of two different drugs, then trial dual therapy:

  • lamotrigine
  • levetiracetam
  • oxcarbazepine
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119
Q

Which anticonvulsants should be avoided in women of child-bearing age?

A
  • sodium valproate
  • topiramate
  • phenobarbital
  • phenytoin
    Enzyme-inducing anticonvulsants lower efficacy of the oral combined contraceptive pill (e.g. carbamazepine).
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120
Q

Options for treatment-resistant epilepsy?

A
  • surgical resection of localised epileptogenic area

- neurostimulation (vagus nerve / deep brain stimulation)

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121
Q

What is meant by status epilepticus?

A

Convulsive seizure lasting > 5 minutes, or repetitive convulsive seizures with no recovery in between.

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122
Q

Causes of status epilepticus?

A
  • anticonvulsant drug withdrawal

- poor anticonvulsant therapy adherence

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123
Q

Pathophysiology of status epilepticus?

A
  • mechanisms that normally abort seizure activity fail, there is excessive and abnormally persistent neuronal excitation
  • neuronal injury occurs due to the accumulation of excitatory neurotransmitters
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124
Q

How is status epilepticus managed?

A
  • ABCDE (secure airway, semi-prone position)
  • supportive care and monitoring
  • IV benzodiazepine (lorazepam)
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125
Q

What is Parkinson’s disease?

A

Chronic, progressive neurodegenerative condition that occurs secondary to loss of dopaminergic neurones within the substantia nigra.

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126
Q

What is meant by Parkinsonism?

A

Refers to the presence of bradykinesia and resting tremor / rigidity / postural instability.

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127
Q

Risk factors for Parkinson’s disease?

A
  • male
  • older age
  • family history
  • head trauma
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128
Q

What is meant by ‘on-off’ fluctuations?

A

Patients switch from dyskinesia to immobility in a few minutes.

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129
Q

What is essential tremor?

A

Progressive, symmetrical movement disorder of the hands and forearms. Absent at rest, present during intentional movements (particularly anti-gravity positions).

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130
Q

Investigations for essential tremor?

A
  • MRI brain

- DaTscan to distinguish between Parkinson’s and essential tremor

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131
Q

What is Huntington’s disease?

A

Autosomal dominant neurodegenerative condition - characterised by chorea, dystonia, and cognitive changes.

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132
Q

Cause of Huntington’s disease?

A

Abnormal expansion of the CAG trinucleotide in the huntingtin gene on chromosome 4.

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133
Q

What is meant by anticipation in Huntington’s disease?

A

More severe disease develops at an earlier age in offspring.

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134
Q

Pathophysiology of Huntington’s disease?

A
  • CAG expansion leads to an elongated polyglutamine tail on the huntingtin protein
  • cleavage and aggregation of this abnormal protein causes neuronal damage
  • loss of neurons results in GABA and ACh depletion, dopamine is spared
  • primarily affects the striatum (caudate and lentiform nuclei)
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135
Q

What does the lentiform nucleus consist of?

A
  • caudate nucleus

- globus pallidus

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136
Q

Clinical manifestations of Huntington’s?

A

Development of psychiatric features and cognitive decline, followed by motor features.

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137
Q

Psychiatric features of Huntington’s?

A
  • depression
  • paranoia / delusions
  • irritability
  • impulsivity
  • disinhibition
  • obsessions and compulsions
  • personality change
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138
Q

Cognitive features of Huntington’s?

A
  • impaired work performance
  • impaired concentration
  • memory loss and dementia
  • difficulties with multi-tasking and complex decisions
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139
Q

Motor features of Huntington’s?

A
  • chorea (abrupt, abnormal, involuntary movements)
  • loss of co-ordination
  • dysphagia and dysarthria
  • dystonia (involuntary muscle contraction causing repetitive or twisting movements)
  • eye movement disorders
140
Q

Investigations for Huntington’s?

A

Genetic testing - PCR analysis and gel electrophoresis.

141
Q

Summary of Huntington’s disease management?

A
  • pharmacological therapies
  • physiotherapy and occupational therapy
  • speech and language therapy
  • neuropsychiatric management
  • palliative care
  • genetic counselling
142
Q

Pharmacological therapies for Huntington’s?

A
  • dopamine depleting agents

- treatment of chorea with anti-psychotics / benzodiazepines

143
Q

Neuropsychiatric management in Huntington’s?

A
  • SSRIs for depression
  • anti-psychotics (e.g. risperidone)
  • CBT
144
Q

Life expectancy in Huntington’s?

A

15-20 years from symptoms onset.

145
Q

Common causes of death in Huntington’s?

A
  • respiratory disease (e.g. pneumonia)

- suicide

146
Q

What is the definition of dementia?

A

Syndrome characterised by a significant deterioration in mental function, leading to impairment of normal function and ability to carry out ADLs.

147
Q

What is the most common cause of dementia?

A

Alzheimer’s (50-75% of cases)

148
Q

Risk factors for Alzheimer’s?

A
  • older age
  • CVD risk factors
  • depression
  • head trauma
  • low social engagement and support
  • Down’s syndrome
  • cerebrovascular disease
149
Q

Why is Down’s syndrome associated with AD?

A

Amyloid precursor protein (APP) gene is found of chromosome 21.

150
Q

Pathophysiology of AD?

A
  • formation of senile plaques and neurofibrillary tangles in the hippocampus and medial temporal lobes
  • senile plaques are extracellular deposits of aggregated beta-amyloid, formed from the breakdown of APP
  • neurofibrillary tangles are intracellular aggregations of hyperphosphorylated tau protein, which promote neuronal death
151
Q

Clinical presentation of AD?

A

Memory impairment is the initial presentation - short term memory loss and difficulty learning new information.

152
Q

Signs and symptoms of AD?

A
  • memory loss
  • disorientation
  • nominal dysphasia
  • apathy
  • personality and mood changes
  • psychiatric problems
  • disinhibition
  • loss of higher cognitive function (multitasking and complex tasks)
153
Q

Cognitive testing in AD?

A

Mini mental state examination (score out of 30). 0-17 is considered severe cognitive impairment.

154
Q

Investigations for AD?

A
  • MMSE / neuropsychological testing
  • head CT / MRI
  • fluorodeoxyglucose-PET to localise areas of brain involvement
  • lumbar puncture and CSF analysis (may show amyloid / tau biomarkers)
155
Q

Which areas of the brain are affected by AD?

A

Hippocampus and medial temporal lobes.

156
Q

Pharmacological therapy for AD?

A
  • acetylcholinesterase inhibitors (donepezil, rivastigmine)

- memantine for severe AD

157
Q

What is frontotemporal dementia?

A

Neurodegenerative disorder characterised by focal degeneration of the frontal and temporal lobes. Causes disturbances in behaviour, personality and language.

158
Q

Epidemiology of frontotemporal dementia?

A
  • common cause of early onset dementia (< 65 years)

- accounts for 2% of dementia cases

159
Q

Cause of frontotemporal dementia?

A

Strong genetic predisposition.

160
Q

Which variant of FTD is more common?

A

Behavioural

161
Q

Pathophysiology of FTD?

A
  • neuronal loss results in frontal / temporal lobe degeneration
  • abnormal protein inclusions may be seen in neurons and glial cells (hyperphosphorylated tau)
162
Q

Clinical manifestations of the behavioural variant of FTD?

A
  • disinhibition
  • loss of empathy
  • apathy
  • compulsive behaviour
163
Q

Clinical manifestations of primary progressive aphasia?

A
  • effortful speech
  • halting speech
  • articulation difficulties
  • word-finding difficulty
164
Q

What are the subtypes of FTD?

A
  • behavioural variant

- primary progressive aphasia

165
Q

Investigations for FTD?

A
  • cognitive assessment (MMSE)

- MRI brain

166
Q

Management of FTD?

A
  • SSRIs for difficult behavioural symptoms
  • occupational therapy
  • physiotherapy
  • speech and language therapy
167
Q

What is Lewy body dementia?

A

Rapidly progressive dementia characterised by Lewy body (alpha-synuclein) deposition in the brain.

168
Q

Clinical manifestations of Lewy body dementia?

A
  • cognitive impairment (difficulties multitasking and performing complex tasks)
  • visual hallucinations
  • Parkinson-like symptoms
169
Q

What is vascular dementia?

A

Common form of dementia caused by cerebrovascular disease.

170
Q

What is mixed dementia?

A

Combination of Alzheimer’s and vascular dementia.

171
Q

How many cases of dementia are vascular?

172
Q

Causes of vascular dementia?

A
  • ischaemic stroke
  • multiple small cerebrovascular infarcts
  • small vessel disease (atherosclerosis)
  • haemorrhage
  • amyloid deposition in small arteries
173
Q

Risk factors for vascular dementia?

A
  • age > 60
  • hypertension
  • smoking
  • hypercholesterolaemia
  • diabetes
174
Q

Clinical presentation of vascular dementia?

A

Stepwise cognitive decline.

175
Q

Signs and symptoms of vascular dementia?

A
  • poor memory
  • dysphasia
  • impaired higher cognitive function (planning and problem-solving)
  • disorientation
  • agitation
  • depression and anxiety
  • disinhibition
  • disturbed sleep cycle
  • apathy
  • focal neurological signs (due to previous stroke)
176
Q

Investigations for vascular dementia?

A
  • cognitive assessment tool (MMSE)

- MRI head

177
Q

Management of vascular dementia?

A
  • control CVD risk factors
  • pharmacological therapies (most useful in patients with mixed dementia)
  • group cognitive stimulation programmes
  • physical activity
178
Q

What is the definition of migraine?

A

Chronic, episodic neurological disorder that causes headache and other associated symptoms. May occur with or without aura.

179
Q

What might trigger a migraine?

A
  • stress
  • bright lights
  • strong smells
  • certain foods
  • dehydration
  • menstruation
  • disturbed sleep patterns
180
Q

Pathophysiology of migraine?

A
  • neurogenic inflammation of first-division (ophthalmic) trigeminal sensory neurons that innervate the meninges and large vessels of the brain
  • activated trigeminal neurons release substances causing sensitisation of peripheral nociceptors and subsequently central sensitisation
181
Q

What causes aura in migraine?

A

Neuronal dysfunction results in waves of neuronal excitation spread anteriorly in the cortex.

182
Q

Signs and symptoms of migraine?

A
  • prolonged headache of moderate / severe intensity
  • nausea and vomiting
  • sound sensitivity and photosensitivity
  • aura
  • throbbing sensation
183
Q

Is migraine unilateral or bilateral?

A

Most commonly unilateral, but over 40% are bilateral.

184
Q

What are some examples of aura?

A
  • visual sparkles, flashing lights
  • visual loss or blind spots
  • numbness / tingling of the face or hands
  • dysphasia may occur
185
Q

What is a hemiplegic migraine?

A

Stroke mimic:

  • hemiplegia
  • ataxia
  • changes in consciousness
186
Q

Investigations for migraine?

A

To exclude differentials:

  • lumbar puncture and CSF analysis
  • CT / MRI head
187
Q

Management of migraines?

A
  1. NSAID + anti-emetic + hydration
  2. paracetamol + anti-emetic + hydration
  3. paracetamol/aspirin/caffeine + anti-emetic + hydration
    Severe symptoms - triptans (serotonin receptor agonists).
    Lifestyle measures - regular meals, sleep hygiene, avoid triggers, etc.
188
Q

What is 5-HT?

189
Q

How do triptans work in migraines?

A
  • cause vasoconstriction of arteries by acting on smooth muscle
  • inhibit the activation of peripheral pain receptors
  • reduce neuronal activity
190
Q

What are tension headaches?

A

Episodic or chronic headaches, pain is like a tight band around the head.

191
Q

Causes of tension headaches?

A
  • stress

- disturbed sleep patterns

192
Q

What are cluster headaches?

A

Unilateral headaches lasting 15-180 minutes, associated with autonomic symptoms.
Considered one of the most painful conditions known.

193
Q

Pathophysiology of cluster headaches?

A
  • trigeminal nerve carries nociceptive information from pain-sensitive structures in the face to the brainstem
  • from the brainstem, information is sent to the cortex via pain-processing pathways after synapsing in the trigeminocervical complex
  • afferent trigeminal signals arriving at the trigeminocervical complex activates the cranial parasympathetic nervous system
194
Q

Signs and symptoms of cluster headaches?

A
  • repeated attacks of excruciating unilateral pain lasting 15-180 minutes
  • nausea and vomiting
  • photophobia / phonophobia
  • aura
  • autonomic features (lacrimation, rhinorrhoea, etc)
195
Q

Acute management of cluster headaches?

A
  • subcutaneous sumatriptan

- oxygen therapy

196
Q

Long-term management of cluster headaches?

A
  • corticosteroid transitional therapy
  • preventative therapy: verapamil
  • deep brain stimulation
197
Q

What is idiopathic intracranial hypertension?

A

Disorder caused by chronically elevated ICP - leading to headache, papilloedema, and vision loss.

198
Q

Typical idiopathic intracranial hypertension patient?

A

Female, obese, child-bearing age.

199
Q

Signs and symptoms of IIH?

A
  • headache (worse lying down or bending over)
  • transient vision loss
  • vision loss
  • photopsia (flashes of light)
  • tinnitus
  • papilloedema
  • diplopia (due to CN VI palsy)
200
Q

Investigations for IIH?

A
  • lumbar puncture (high opening pressure)
  • fundoscopy
  • MRI brain
201
Q

Signs of papilloedema on fundoscopy?

A
  • venous engorgement
  • loss of venous pulsation
  • haemorrhages adjacent to optic disc
  • blurring of optic margins
202
Q

Management of IIH?

A
  • weight loss (with low sodium diet)
  • serial lumbar punctures
  • carbonic anhydrase inhibitor (to reduce production of CSF)
  • furosemide
  • neurosurgical interventions
203
Q

What is giant cell arteritis?

A

Systemic granulomatous vasculitis primarily affecting branches of the external carotid artery. Symptoms typically affect the temporal artery.

204
Q

What disease is associated with giant cell arteritis?

A

Polymyalgia rheumatica

205
Q

What is polymyalgia rheumatica?

A

Inflammatory disorder causing pain and stiffness in the muscles around the shoulders, neck, and hips.

206
Q

Pathophysiology of GCA?

A
  • immune insult occurs in the outer (adventitial) layer of the arterial wall
  • dendritic cells attract T cells and present antigens to them
  • T helper cells enter the artery via the vasa vasorum, become activated and undergo clonal expansion in the artery wall
  • T cells release interferon gamma which stimulates macrophages and induces multinucleated giant cell formation
  • macrophages release cytokines, causing damage to the arterial wall
  • the artery releases growth and angiogenic factors, leading to intimal expansion and hyperplasia
  • this results in narrowing and occlusion of the vessel lumen, causing ischaemia
207
Q

Histological appearance of GCA?

A

Arteries contain inflammatory skip lesions composed of T cells and macrophages. Multinucleated giant cells are present in around 50% of cases.

208
Q

Signs and symptoms of GCA?

A
  • severe unilateral headache around the temple
  • amaurosis fugax / blurred vision / vision loss
  • arterial thickening / nodularity
  • scalp tenderness
  • jaw claudication
  • muscle aches and stiffness in shoulders, neck and hips
209
Q

Gold standard investigation for GCA?

A

Temporal artery biopsy.

210
Q

Investigations for GCA?

A
  • temporal artery biopsy
  • CRP / ESR
  • vascular ultrasound - wall thickening (‘halo’ sign), stenosis, occlusion
211
Q

Management of GCA?

A
  • high dose corticosteroids (reduce risk of site loss)
  • aspirin 75mg daily
  • bone and gastric protection (bisphosphonates, PPI)
212
Q

Complications of GCA?

A
  • stroke

- vision loss

213
Q

What is trigeminal neuralgia?

A

Facial pain syndrome in the distribution of one or more divisions of the trigeminal nerve. Characterised by paroxysms of sharp, stabbing pain, or a constant component of facial pain.

214
Q

Causes of trigeminal neuralgia?

A

Classical - vascular compression of the trigeminal root by tortuous or aberrant vessels.
Symptomatic - caused by a structural lesion such as a tumour or MS.

215
Q

Pathophysiology of trigeminal neuralgia?

A

Neuropathic pain is caused by focal demyelination of trigeminal neurons, resulting in conduction abnormalities.

216
Q

Management of trigeminal neuralgia?

A
  • anticonvulsant (carbamazepine)

- microvascular decompression surgery

217
Q

What is cauda equina syndrome?

A

Compression of the collection of nerves distal to the terminal part of the spinal cord. Syndrome characterised by lower limb weakness, bladder and bowel dysfunction, and abnormal perianal sensation.

218
Q

What vertebral level does the cauda equina start?

219
Q

What nerve roots does the cauda equina contain?

220
Q

Causes of cauda equina syndrome?

A
  • lumbar stenosis (narrowing of the spinal canal)
  • spinal trauma
  • disc herniation
  • malignancy
  • spinal infections (e.g. abscess)
  • neural tube defects
221
Q

Is cauda equina syndrome an UMN lesion or a LMN lesion?

A

LMN lesion

222
Q

Signs and symptoms of cauda equina syndrome?

A
  • lower back pain
  • asymmetrical sciatica pain (alternating buttock pain)
  • saddle anaesthesia
  • bladder dysfunction (urinary retention / overflow incontinence)
  • bowel dysfunction (constipation, incontinence, loss of anal tone)
  • asymmetrical lower limb weakness / sensory changes
  • hypotonia and hyporeflexia
223
Q

Gold standard investigation for cauda equina syndrome?

224
Q

Management of cauda equina syndrome?

A

Neurosurgical emergency requiring decompressive surgery.

225
Q

Complications of cauda equina syndrome?

A
  • bladder and bowel dysfunction
  • sexual dysfunction
  • chronic pain
  • paralysis
226
Q

What is multiple sclerosis?

A

Chronic, progressive condition involving demyelination of neurons in the CNS. Caused by autoimmune activation against myelin and subsequent inflammation.

227
Q

Definition of MS?

A

The presence of episodic neurological dysfunction in at least two areas of the CNS, separated in space and time.

228
Q

What is progressive-relapsing MS?

A

Progressive worsening of the condition from the beginning, with distinct attacks of symptoms occurring throughout the course of the disease.

229
Q

What is secondary progressive multiple sclerosis?

A

Initially follows a relapsing-remitting course, then there is progressive worsening.

230
Q

What is primary progressive MS?

A

Progressive worsening of the condition from the beginning, without distinct attacks of symptoms.

231
Q

What is relapsing-remitting MS?

A

Distinct attacks of symptoms partially resolve, leaving residual disability. Subsequent attacks cause an increase in disability. There is no progression of the condition between the attacks.

232
Q

Cause of MS?

A

Autoimmune disease - combination of genetic factors and environmental triggers.

233
Q

Typical MS patient?

A

Female, aged 20-40.

234
Q

What type of hypersensitivity reaction is involved in MS?

A

Type IV - cell-mediated.

235
Q

Pathophysiology of MS?

A
  • T cell crosses the BBB and becomes activated by myelin
  • activated T cell causes upregulation of endothelial adhesion molecules, allowing passage of more immune cells across the BBB
  • T cell releases cytokines, attracting B cells and macrophages
  • B cells produce antibodies against myelin
  • macrophages phagocytoses oligodendrocytes
  • destruction of oligodendrocytes causes demyelination of axons, leaving areas of scar tissue (plaques)
236
Q

Pathophysiology of relapsing-remitting MS?

A
  • regulatory T cells act to inhibit the immune response and reduce inflammation
  • this allows remyelination to occur in early MS
  • eventually irreversible damage and permanent demyelination occur
237
Q

What are some clinical manifestations of MS?

A
  • optic neuritis
  • eye movement abnormalities
  • focal weakness (Bell’s palsy, Horner syndrome, limb paralysis, incontinence)
  • focal sensory symptoms (trigeminal neuralgia, numbness / paraesthesia)
  • ataxia
238
Q

What is the most common presentation of MS?

A

Optic neuritis

239
Q

What are some features of optic neuritis?

A
  • central scotoma (blind spot)
  • pain on eye movement
  • impaired colour vision
240
Q

What is Horner syndrome?

A

Unilateral:

  • ptosis
  • miosis (constricted pupil)
  • anhidrosis (absence of sweating)
241
Q

Investigations for MS?

A
  • MRI brain
  • lumbar puncture with CSF electrophoresis (shows oligoclonal IgG bands)
  • visual evoked potential - measures speed of nerve impulses along the optic nerve in response to visual stimuli
242
Q

Differentials for MS?

A
  • ischaemic stroke
  • Guillian-Barre syndrome
  • vitamin B12 deficiency
  • fibromyalgia
243
Q

What are some disease-modifying drugs for MS?

A
  • recombinant interferon beta (interferes with demyelinating plaque formation)
  • immunosuppressants
244
Q

Treatment for MS relapse?

A

Methylprednisolone

245
Q

Treatment for spasticity in MS?

A
  • baclofen
  • gabapentin
  • physiotherapy
246
Q

What is myasthenia gravis?

A

Chronic autoimmune disorder of the post-synaptic membrane at the neuromuscular junction in skeletal muscle. Characterised by muscle weakness and fatiguability.

247
Q

What is the bimodal peak in incidence for myasthenia gravis?

A
  • females aged 20-30

- males aged 60-70

248
Q

What type of hypersensitivity reaction is involved in myasthenia gravis?

A

Type II (antibody mediated).

249
Q

Pathophysiology of myasthenia gravis?

A
  • anti AChR antibodies bind to ACh-R on the motor end plate of skeletal muscle, blocking the binding of ACh
  • there is a reduction in the number of ACh receptors on the post-synaptic membrane
  • complement-mediated destruction of the post-synaptic membrane reduces the surface area available for new ACh-R insertion
250
Q

What are some ocular manifestations of myasthenia gravis?

A
  • diplopia

- ptosis

251
Q

What are some respiratory manifestations of myasthenia gravis?

A
  • breathlessness
  • weak breathing
  • respiratory failure
252
Q

What are some bulbar manifestations of myasthenia gravis?

A
  • fatiguable chewing
  • dysarthria
  • dysphagia
253
Q

What are some limb manifestations of myasthenia gravis?

A
  • dropped head
  • proximal affected more than distal
  • arms affected more than legs
254
Q

What is the ice pack test?

A

Improvement in ptosis after the application of an ice pack to the closed eyelids for 2 minutes.

255
Q

What is myasthenic crisis?

A

Worsening of muscle weakness requiring respiratory support.

256
Q

Investigations for myasthenic crisis?

A
  • serum anti-AChR antibodies / anti-MuSK antibodies
  • repetitive nerve stimulation / electromyography
  • ice pack test
  • CT / MRI chest (to assess thymus gland)
257
Q

Management of myasthenia gravis?

A
  • acetylcholinesterase inhibitor (pyridostigmine)
  • corticosteroids (prednisolone)
  • immunosuppressants (azathioprine)
  • thymectomy - if patients have thymoma
258
Q

Side effects of pyridostigmine?

A
  • diarrhoea
  • urinary incontinence
  • GI upset
  • bronchospasm
  • sweating
259
Q

How is myasthenic crisis managed?

A
  • HDU / ITU admission
  • respiratory support if needed (intubation and ventilation)
  • IVIG and plasma exchange
  • prednisolone
260
Q

What is Lambert Eaton myasthenic syndrome?

A

Autoimmune disorder of the neuromuscular junction. Characterised by the presence of circulating antibodies against voltage-gated calcium channels.

261
Q

What causes LEMS?

A
  • paraneoplastic syndrome (e.g. associated with small cell lung cancer)
  • non-paraneoplastic LEMS occurs due to a general autoimmune state
262
Q

Pathophysiology of LEMS?

A
  • antibodies are produced against voltage-gated calcium channels
  • anti-VGCC antibodies damage the calcium channels in the presynaptic terminals of the neuromuscular junction
  • this inhibits the release of ACh into the synaptic cleft, inhibiting muscle contraction
263
Q

Signs and symptoms of LEMS?

A
  • limb weakness (proximal)
  • dysarthria
  • ptosis and diplopia
  • dysphagia
  • autonomic symptoms: dry mouth, orthostatic hypotension, erectile dysfunction
264
Q

Investigations for LEMS?

A
  • repetitive nerve stimulation / electromyography
  • serum anti-VGCC antibodies
  • imaging tests for small cell lung cancer (CT, MRI, PET)
265
Q

Management of LEMS?

A
  • manage underlying malignancy
  • amifampridine - allows release of more ACh into the synaptic cleft
  • immunosuppressants (prednisolone / azathioprine)
  • IVIG
  • plasma exchange
266
Q

Mechanism of action of amifampridine?

A

Blocks voltage-gated potassium channels in the pre-synaptic terminal, prolonging the depolarisation of the cell membrane to allow the release of more ACh into the synaptic cleft.

267
Q

What is Guillain-Barré syndrome?

A

Acute inflammatory polyneuropathy - characterised by a progressive, symmetrical, ascending neuropathy resulting in weakness and reduced reflexes. The majority of patients have a history of preceding illness.

268
Q

Infective causes of GBS?

A
  • campylobacter jejuni
  • cytomegalovirus
  • Epstein-Barr virus
269
Q

What is the pathophysiology of GBS?

A
  • immune-mediated damage to peripheral nerves
  • ‘molecular mimicry’ occurs, where antibodies generated in response to pathogens cross-react with the body’s nerve cells
  • antibodies target the myelin sheath
270
Q

Clinical manifestations of GBS?

A
  • progressive symmetrical weakness in limbs, ascending from distal muscles
  • respiratory muscle involvement
  • reduced tendon reflexes
  • reduced sensation / paraesthesia
271
Q

What is Miller Fisher syndrome?

A

GBS variant characterised by:

  • ataxia
  • areflexia
  • ophthalmoplegia
272
Q

What is ophthalmoplegia?

A

Paralysis of extraocular muscles due to involvement of CN III, IV or, VI.
Diplopia is a characteristic symptom.

273
Q

Investigations for GBS?

A
  • lumbar puncture
  • antibody screen (anti-GQ1b is specific for Miller Fisher syndrome)
  • spirometry to monitor respiratory function
  • nerve conduction studies / electromyography
274
Q

What is electromyography?

A

Measures electrical activity in response to a nerve’s stimulation of muscle. Involves the insertion of electrodes (needles) through the skin into the muscle.

275
Q

Gold standard for GBS diagnosis?

A

Lumbar puncture - high CSF protein with normal CSF WCC.

276
Q

Management of GBS?

A
  • IVIG
  • plasma exchange
  • ventilation
277
Q

Complication of GBS?

A

Respiratory failure.

278
Q

Contraindications for lumbar puncture?

A
  • raised ICP
  • decreased GCS
  • coagulopathy
  • infection at the site of lumbar puncture
279
Q

What is carpal tunnel syndrome?

A

Entrapment of the median nerve against the carpal tunnel.

280
Q

Risk factors for carpal tunnel syndrome?

A
  • diabetes
  • osteoarthritis
  • obesity
  • hypothyroidism
  • pregnancy
  • trauma
281
Q

Pathophysiology of carpal tunnel syndrome?

A
  • anatomical compression of the median nerve occurs due to flexor tendon fibrosis, a mass lesion, or an anatomically small tunnel
  • inflammation of the median nerve occurs in response to the compressive injury
282
Q

Sensory innervation provided by the median nerve?

A

Palmar and distal dorsal aspects of the lateral three-and-a-half digits.

283
Q

Motor innervation provided by the median nerve?

284
Q

Nerve roots of the median nerve?

A

C6, C7, C8, T1

285
Q

Signs and symptoms of carpal tunnel syndrome?

A
  • dull ache / discomfort in wrist, fingers, or forearm
  • paraesthesia
  • weakness
  • clumsiness & difficulty opening jars, buttoning shirts, etc.
  • sensory loss
  • thenar eminence wasting
  • weak thumb abduction and opposition
286
Q

Management of carpal tunnel syndrome?

A
  • wrist splints
  • physiotherapy
  • corticosteroids
  • open / laparoscopic carpal tunnel release
287
Q

Features of UMN lesion?

A
  • hypertonia
  • hyperreflexia
  • spasticity
  • Babinski reflex
  • ankle clonus
  • jaw clenching
288
Q

Features of LMN lesion?

A
  • hypotonia
  • hyporeflexia
  • fasciculations
  • muscle cramps
  • muscle atrophy
  • weakness
289
Q

Key mutations in familial MND?

A
  • C9orf72

- SOD-1

290
Q

Pathophysiology of MND?

A
  • progressive degeneration of both upper and lower motor neurons
  • sensory neurons are spared
291
Q

Pharmacological therapy for MND?

A
  • riluzole (anti-glutamate medication)
  • baclofen for muscle cramps
  • opioid therapy for breathlessness
292
Q

What is Bell’s palsy?

A

Unilateral facial nerve palsy of known cause.

293
Q

What is the most common cause of facial palsy?

A

Bell’s palsy

294
Q

Presentation of Bell’s palsy?

A

Rapid onset (< 72 hours) of unilateral facial weakness.

295
Q

Signs and symptoms of Bell’s palsy?

A
  • unilateral facial weakness
  • post-auricular / ear pain
  • difficulty chewing
  • drooling
  • incomplete eye closure
  • hyperacusis
  • loss of nasolabial fold (smile lines)
  • no forehead sparing
  • eyebrow drooping
  • asymmetrical smile
296
Q

Why is there no forehead sparing in Bell’s palsy?

A

LMN lesion

297
Q

What is Bell’s sign?

A

Upward movement of the eye on attempt to close the eye.

298
Q

Why does hyperacusis occur in Bell’s palsy?

A

Involvement of the nerve supplying the stapedius muscle.

299
Q

Recovery time for Bell’s palsy?

A

Most patients make a full recovery within 4 months.

300
Q

Management of Bell’s palsy?

A

Prednisolone if patients present within 72 hours of onset.
Eye care: lubricating drops, tape eye shut when sleeping, wear sunglasses outdoors.
Straw for liquids and soft diet if chewing affected.

301
Q

Cause of Bell’s palsy?

A

Thought to be related to inflammation and oedema of the facial nerve secondary to a viral infection or autoimmunity.

302
Q

Anti-emetic example?

A

Ondansetron - 5-HT 3 receptor antagonist.

303
Q

What is Paget’s disease?

A

Chronic bone disorder characterised by focal areas of increased bone remodelling (increased osteoclast and osteoblast activity). This leads to osseous deformities, altered joint biomechanics, nerve compressions and pathological fractures.

304
Q

Signs and symptoms of Paget’s disease?

A
  • long bone or back pain
  • pathological fractures
  • boney deformities (frontal bossing, prognathism, etc)
  • hearing loss (skull involvement affecting CN VIII)
  • facial pain (CN V)
305
Q

Management of Paget’s disease?

A
  • bisphosphonates
  • second line: calcitonin
  • physiotherapy, analgesia, hearing aids
306
Q

Where do primary brain tumours typically originate in adults?

A

Supratentorial (cerebrum).

307
Q

Where do primary brain tumours typically originate in children?

A

Posterior fossa.

308
Q

Types of glioma?

A
  • astrocytoma
  • oligodendroma
  • ependymoma
309
Q

Most common type of astrocytoma?

A

Glioblastoma

310
Q

How aggressive are gliomas?

A

Graded from 1-4. 4 is most aggressive (e.g. glioblastoma).

311
Q

What are some effects of meningiomas?

A

Usually benign, but mass effect can lead to raised ICP.

312
Q

What are some effects of pituitary tumours?

A
  • usually benign
  • compression of optic chiasm (macroadenoma), leading to bitemporal hemianopia
  • hypopituitarism
  • excessive release of hormones (acromegaly, Cushing’s disease, etc)
313
Q

What is medulloblastoma?

A

Most common malignant brain tumour in children, arising from / near the cerebellum.

314
Q

What is meningitis?

A

Inflammation of the meninges, usually due to a bacterial or viral infection.

315
Q

What is meningococcal septicaemia?

A

Meningococcal bacterial infection present in the bloodstream. Causes disseminated intravascular coagulation and subcutaneous haemorrhage.

316
Q

Is meningitis usually viral or bacterial?

317
Q

Bacterial causes of meningitis?

A
  • neisseria meningitidis
  • streptococcus pneumoniae
  • listeria monocytes (in elderly / immunocompromised)
318
Q

Most common cause of meningitis in neonates?

A

Group B streptococcus

319
Q

Viral causes of meningitis?

A
  • enteroviruses
  • herpes viruses
  • mumps virus
  • measles virus
320
Q

Examples of herpes viruses?

A
  • herpes simplex virus
  • varicella zoster virus
  • Epstein-Barr virus
321
Q

Signs and symptoms of meningitis?

A
  • fever
  • headache
  • neck stiffness
  • nausea & vomiting
  • photophobia
  • altered consciousness
  • seizures
  • raised ICP (papilloedema and focal neurological signs)
  • Kernig’s and Brudzinski’s signs
322
Q

Which type of meningitis is most likely to cause raised ICP?

323
Q

What is Kernig’s sign?

A

Lower back pain on extension of knee when hip is flexed at 90 degrees. Due to stretch of the meninges.

324
Q

What is Brudzinski’s sign?

A

Patient lies on their back, flexion of the neck (lifting) causes reflex flexion of the hips.

325
Q

Which type of meningitis is most likely to cause Kernig’s / Brudzinski’s signs?

326
Q

Investigations for meningitis?

A
  • blood culture
  • viral stool and throat swab
  • lumbar puncture and CSF analysis
  • CT head BEFORE lumbar puncture if risk of cerebral herniation
327
Q

CSF appearance viral vs bacterial?

A

bacterial - cloudy

viral - clear

328
Q

CSF protein viral vs bacterial?

A

bacterial - high

viral - normal / mild elevation

329
Q

CSF glucose viral vs bacterial?

A

bacterial - low

viral - normal

330
Q

CSF WBCs viral vs bacterial?

A

bacterial - high neutrophils

viral - high lymphocytes

331
Q

Empirical antibiotics for bacterial meningitis?

A
  • cefotaxime / ceftriaxone
332
Q

What additional empirical antibiotic should be used if there is a risk of listeria meningitis?

A

Ampicillin

333
Q

Additional drug to treat bacterial meningitis, in addition to antibiotics?

A

Dexamethasone - to reduce neurological damage.

334
Q

Post-exposure prophylaxis for contacts of bacterial meningitis?

A

Ciprofloxacin

335
Q

Management of viral meningitis?

A
  • supportive care

- aciclovir may be used for herpes virus infection

336
Q

Definition of encephalitis?

A

Inflammation of the brain parenchyma, usually caused by viruses.

337
Q

Most common viral cause of encephalitis?

A

Herpes viruses are the most common group (herpes simplex virus, varicella zoster virus, cytomegalovirus, Epstein-Barr virus).
Herpes simplex virus type 1 is the most common cause.

338
Q

Route of encephalitis infection?

A
  • virus gains entry and replicates in local or regional tissue
  • virus then reaches the CNS by haematogenous spread or retrograde axonal transport
339
Q

Signs and symptoms of encephalitis?

A
  • fever
  • altered mental state
  • focal neurological deficits
  • seizures
  • signs of causative viral infection (rash / cough / GI upset)
340
Q

Gold standard investigation for encephalitis?

A

Lumbar puncture and CSF analysis (with viral PCR testing).

341
Q

Management of encephalitis?

A
  • empirical antiviral therapy (aciclovir)

- supportive measures

342
Q

Management of Wernicke’s encephalopathy?

A
  • IV thiamine

- IV magnesium sulfate

343
Q

Inheritance of Duchenne muscular dystrophy?

A

X-linked recessive

344
Q

Pathophysiology of Duchenne muscular dystrophy?

A

Absence of dystrophin.

345
Q

What is risperidone?

A

Anti-psychotic

346
Q

What is conus medullaris syndrome?

A

Spinal cord injury at the level of the conus medullaris (L1) - results in UMN signs.

Phase 2a (10 decks)

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